This research endeavor is aimed at understanding the effects of cardiac bypass on the fetus, with the hope that this knowledge will contribute to the development of safe corrective surgery for congenital heart disease in the human fetus. The advantages of early surgical intervention are obvious in defects that would require a much more challenging repair after birth. Prenatal repair would prevent the subsequent development of complex lesions during the fetal period. However, a detailed understanding of the effect of cardiac surgery and extracorporeal circulation on the fetus is required. The focus of this project is to identity the inflammatory mediators responsible for the fetal and placental pathophysiologic response to cardiac bypass using a fetal primate model. The role of cytokines, eicosanoids, and autocoids as candidate mediators of fetal and placental dysfunction will be examined. The effectiveness of attenuating this response with pharmacological antagonists of these putative mediators will also be explored.